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Iodine Deficiency

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD  more...
Updated: Dec 16, 2015


Severe iodine deficiency results in impaired thyroid hormone synthesis and/or thyroid enlargement (goiter). Population effects of severe iodine deficiency, termed iodine deficiency disorders (IDDs), include endemic goiter, hypothyroidism, cretinism, decreased fertility rate, increased infant mortality, and mental retardation. (See Pathophysiology and Presentation.)[1]

Iodine is a chemical element. It is found in trace amounts in the human body, in which its only known function is in the synthesis of thyroid hormones. Iodine is obtained primarily through the diet but is also a component of some medications, such as radiology contrast agents, iodophor cleansers, and amiodarone. (See Etiology.)

Worldwide, the soil in large geographic areas is deficient in iodine. Twenty-nine percent of the world’s population, living in approximately 130 countries, is estimated to live in areas of deficiency (see the Table).[2] This occurs primarily in mountainous regions such as the Himalayas, the European Alps, and the Andes, where iodine has been washed away by glaciation and flooding. Iodine deficiency also occurs in lowland regions far from the oceans, such as central Africa and Eastern Europe. Persons who consume only locally produced foods in these areas are at risk for IDD. See the distribution of iodine deficiency in the image below. (See Epidemiology.)

Distribution of iodine deficiency in developing co Distribution of iodine deficiency in developing countries.


Table. (Open Table in a new window)

Iodine Deficiency None Mild Moderate Severe
Median urine iodine, mcg/L >100 50-99 20-49 < 20
Goiter prevalence < 5% 5-20% 20-30% >30%
Neonatal thyroid-stimulating hormone (TSH),

>5 IU/mL whole blood

< 3% 3-20% 20-40% >40%
Cretinism 0 0 + +
Adapted from the World Health Organization (WHO)/United Nations Children's Fund (UNICEF)/International Council for Control of Iodine Deficiency Disorders (ICCIDD).


Normal dietary iodine intake is 100-150 mcg/day. The US Institute of Medicine’s (IOM’s) recommended dietary allowance (RDA) of iodine is as follows:

  • Adults and adolescents - 150 mcg/day
  • Pregnant women - 220 mcg/day
  • Lactating women - 290 mcg/day
  • Children aged 1-11 years - 90-120 mcg/day
  • Infants - Adequate intake is 110-130 mcg/day

WHO’s recommendations are similar, although the organization recommends 200 mcg/day for pregnant or lactating women and 50-90 mcg/day for infants younger than 1 year.[3]

Sources of dietary iodine

In areas where iodine is not added to the water supply or food products meant for humans or domesticated animals, the primary sources of dietary iodine are saltwater fish, seaweed, and trace amounts in grains. The upper limit of safe daily iodine intake is 1100 mcg/day for adults; it is lower for children.[4, 5, 6, 7]

In the United States, iodine has been voluntarily supplemented in table salt (70 mcg/g). Salt was selected as the medium for iodine supplementation because intake is uniform across all socioeconomic strata and across seasons of the year, supplementation is achieved using simple technology, and the program is inexpensive. The estimated annual cost of iodine supplementation of salt in the United States is $0.04 per person. (See Treatment and Medication.)

Other major sources of dietary iodine in the United States are egg yolks, milk, and milk products because of iodine supplementation in chicken feed, the treatment of milk cows and cattle with supplemental dietary iodine to prevent hoof rot and increase fertility, and the use of iodophor cleaners by the dairy industry.[8]

Changes in US iodine intake

In the early 1900s, the Great Lakes, Appalachian, and northwestern regions of the United States were endemic regions for IDD, but since the iodization of salt and other foods in the 1920s, dietary iodine levels generally have been adequate. However, sustaining these iodization programs has become a concern.

Data collected in the United States by National Health and Nutrition Examination Survey I (NHANES I) for the years 1971-1974 showed that the median urinary iodine level was 320 mcg/L, reflecting adequate dietary iodine intake.[9] However, by the time of NHANES III (1988-1994), the median urinary iodine value had fallen to 145 mcg/L.

The reduction in US dietary iodine intake since the 1970s has likely been the result of the removal of iodate conditioners in store-bought breads, widely publicized recommendations for reduced salt and egg intake for blood pressure and cholesterol control, the increasing use of noniodized salt in manufactured or premade convenience foods, decreased iodine supplementation of cattle feed, poor education about the medical necessity of using iodized salt, and reduction in the number of meals made at home.[9, 10, 11]

The NHANES surveys of 2001-2002, 2005-2006, and 2007-2008 showed that US dietary iodine intake has stabilized.[10, 11] Although the most recent NHANES survey reveals adequate iodine intake in the general US population, certain groups have an insufficient intake of iodine, such as pregnant women, who were found to have a median urinary iodine concentration of 125 mcg/L).[12]

Population-based assessment and treatment

In population-based assessments, iodine sufficiency can be determined based on the results of a spot urine test for iodine and creatinine.[10] Supplementation can be achieved by using iodized salt in cooking or a once-daily multiple vitamin containing sodium iodide. (See Workup, Treatment, and Medication.)[4, 13]

Pediatric considerations

Iodine stores within the thyroid increase with age in pediatric patients. Therefore, infants and young children tend to have higher131 I uptake than do adults. Additionally, newborns and young infants are much more severely affected by iodine deficiency than are adults and are more likely to become overtly hypothyroid. (See Presentation.)

Prenatal considerations

Women with severe iodine deficiency are more likely to experience infertility, and pregnancy in this group is more likely to result in miscarriage or congenital anomalies. Thyroid hormones are essential for fetal brain growth and development, and severe maternal iodine deficiency may lead to mental and growth retardation or cretinism in offspring, and even mild maternal iodine deficiency has been associated with lower IQ in children.[14] Even in areas of borderline iodine intake, as many as 10% of women may develop goiter during pregnancy. (See Presentation.)

Patient education

The public must understand the importance of using iodized salt, especially in the United States, where iodization of salt is not mandated by law. Several areas of the world, including the United States, Australia, and the Netherlands, where iodine deficiency was eradicated by voluntary methods, have later shown a significant decrease in iodine intake.

For patient education information, see the Thyroid and Metabolism Center and the Pregnancy Center, as well as Thyroid Problems and Miscarriage.



Dietary iodine is taken up readily through the gut in the form of iodide. From the circulation, it is concentrated in the thyroid gland by means of an energy-dependent sodium-iodate symporter. In the follicle cells of the thyroid gland, 4 atoms of iodine are incorporated into each molecule of thyroxine (T4) and 3 atoms into each molecule of triiodothyronine (T3). These hormones are essential for neuronal development, sexual development, and growth and for regulating the metabolic rate, body heat, and energy.

When dietary iodine intake is inadequate for thyroid hormone synthesis, the serum T4 level initially falls and a number of processes ensue to restore adequate thyroid hormone production. The pituitary gland senses low levels of circulating T4 and releases more thyroid-stimulating hormone (TSH). TSH stimulates the growth and metabolic activity of thyroid follicular cells. TSH stimulates each cell to increase iodine uptake and thyroid hormone synthesis and secretion. Increased TSH levels and reduction of iodine stores within the thyroid result in increased T3 production relative to T4 production. T3 is 20-100 times more biologically active than T4 and requires fewer atoms of iodine for biosynthesis. The increased production T 3 results in the maintenance of normal levels of thyroid hormone bioactivity despite the reduction in T 4 because of iodine deficiency.

These processes tend to conserve iodine stores and help maintain normal thyroid function. In addition, thyroid hormones are deiodinated in the liver, and the iodine is released back into the circulation for reuptake and reuse by the thyroid gland. Even under these circumstances, iodine is passively lost in the urine, with additional small (10%) losses from biliary secretion into the gut.

Goiter development and hyperthyroidism

Enlargement of the thyroid gland begins as an adaptive process to low iodine intake. Iodine deficiency is the most common cause of goiter in the world. The goiter initially is diffuse, but it eventually becomes nodular. Some nodules may become autonomous and secrete thyroid hormone regardless of the TSH level. These autonomous nodules have been demonstrated to frequently contain TSH-activating mutations. Initially, thyroid hormone output by the normal thyroid surrounding the autonomous nodules is reduced to maintain euthyroidism. Autonomous nodules may cause hyperthyroidism.

High levels of iodine, such as those found in radiographic contrast dyes or amiodarone, may cause hyperthyroidism in the setting of nodular goiter with “hot” or autonomous nodules or hypothyroidism in the setting of autoimmune thyroid disease. If the total output of thyroid hormone by the autonomous nodules exceeds that of the normal thyroid gland, the patient becomes biochemically hyperthyroid. This condition is known as a toxic multinodular goiter.


When iodine deficiency is more severe, thyroid hormone production falls and the patient may experience a hypothyroid condition. In such cases, adults have the usual signs and symptoms of hypothyroidism. However, congenital hypothyroidism (also known as cretinism) in fetuses and young children prevents central nervous system development and maturation, resulting in permanent mental retardation, neurologic defects, and growth abnormalities.[4, 15]



Occurrence in the United States

Early in the 20th century, the Great Lakes, Appalachian, and northwestern regions of the United States were endemic for iodine deficiency disorders, but since the iodization of salt and other foods in the 1920s, dietary iodine levels generally have been adequate. National survey data suggest that average US dietary iodine intake fell dramatically from 1971-1990 and then stabilized. Urinary iodine values of less than 50 mcg/L, moderate iodine deficiency, are found in 11.1% of the total population, 7.3% of pregnant women, and 16.8% of reproductive-aged women.[9, 10]

International occurrence

Internationally, 2.2 billion people worldwide are at risk for IDD. Of these persons, 30-70% have goiter and 1-10% have cretinism. The clinical disorders of iodine deficiency tend to be more profound in geographic areas associated with coexisting selenium and vitamin A deficiencies and in regions where goitrogens, such as cassava or millet, are major staples of the diet.

Race-, sex-, and age-related demographics

No race predilection exists for IDD; prevalence is affected only by geographic area and diet. After age 10 years, the prevalence of goiter is higher in girls than in boys in areas of iodine deficiency. No sex-based difference is observed in the incidence of cretinism.

Patients of any age can be affected by iodine deficiency. The most devastating complications of iodine deficiency disorder occur when iodine is deficient during fetal and neonatal growth.



The supplementation of iodine does not reverse cretinism or reduce the size of large nodular goiters. Small, diffuse goiters of short duration that occur in infants or during pregnancy appear to be managed effectively with iodine supplementation.

Iodine deficiency can recur if iodine supplementation programs lapse.[16] Recurrence of goiter and new cases of cretinism have been noted in some nations where this has occurred. These changes are manifested prominently in school-aged children, who are particularly sensitive to variations in iodine intake. Thyroid volume, prevalence of goiter, and urinary iodine levels may return to pre-iodine supplementation levels 1-2 years following the discontinuation of iodine supplementation.


Mild to moderate IDD can cause thyroid function abnormalities and endemic goiter. In areas with severe endemic IDD, rates of miscarriage and infant mortality are increased. Cretinism is rare, but populations in which severe iodine deficiency is prevalent are at risk for reduced intelligence and mental retardation. In fact, iodine deficiency is the leading cause of preventable mental retardation worldwide.

Whether iodine deficiency causes an increased risk for thyroid cancer is unclear, but a higher proportion of more aggressive thyroid cancers (ie, follicular thyroid carcinoma) and an increased thyroid cancer mortality rate are found in areas where iodine deficiency is endemic.

Contributor Information and Disclosures

Stephanie L Lee, MD, PhD Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.


Elizabeth N Pearce, MD, MSc Associate Professor of Medicine, Boston Medical Center, Boston University School of Medicine

Elizabeth N Pearce, MD, MSc is a member of the following medical societies: American Association of Clinical Endocrinologists, American Thyroid Association, Endocrine Society, Massachusetts Medical Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: consulted for Scientific Consulting Company GmbH; advisory board for Endocrine Advisor Website; Member of the Management Council of the Iodine Global Network.

Sonia Ananthakrishnan, MD Assistant Professor of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center, Boston University School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.


Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Distribution of iodine deficiency in developing countries.
Typical endemic goiters in 3 women from the Himalayas, an area of severe iodine deficiency. Image courtesy of F. DeLange.
A man and 3 females (age range, 17-20 y) with myxedematous cretinism from the Republic of the Congo in Africa, a region with severe iodine deficiency. Image courtesy of F. DeLange.
Histologic sections from a normal thyroid and from an endemic goiter that was removed because of compressive symptoms. The normal thyroid (A) contains thyroid cells arranged in a monolayered sheet around a storage form of thyroid hormone, colloid, while the endemic goiter (B) shows intense hyperplasia with no colloid. Image courtesy of F. DeLange.
Iodine Deficiency None Mild Moderate Severe
Median urine iodine, mcg/L >100 50-99 20-49 < 20
Goiter prevalence < 5% 5-20% 20-30% >30%
Neonatal thyroid-stimulating hormone (TSH),

>5 IU/mL whole blood

< 3% 3-20% 20-40% >40%
Cretinism 0 0 + +
Adapted from the World Health Organization (WHO)/United Nations Children's Fund (UNICEF)/International Council for Control of Iodine Deficiency Disorders (ICCIDD).
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